This type I diabetic is presenting with signs and symptoms of diabetic ketoacidosis (DKA). In DKA, total body potassium stores are generally decreased due to osmotic diuresis.
DKA is a life-threatening emergency that may occur in either type I or type II diabetics but is significantly more common in patients with type I. The pathogenesis is related to insulin deficiency resulting in hyperglycemia that leads to osmotic diuresis and hypovolemia. The inability of the body to use the available glucose for ATP production results in ketone formation and eventually an anion gap metabolic acidosis. Serum potassium levels may be low, normal, or elevated, but total body stores are generally low and require repletion. Common precipitating factors include infection, trauma, myocardial infarction, sepsis and, of course, inadequate insulin administration. Patients may present with nausea, vomiting, abdominal pain, Kussmaul respirations (rapid, deep breaths), dehydration, polydipsia, polyuria and may eventually progress to altered mental status.
Trachtenbarg discusses DKA. Diagnosis requires glucose greater than 250 mg/dL, pH less than 7.3, and bicarbonate less than 18 mEq/L. Beta-hydroxybutyrate is a better measurement of ketosis than serum ketones. Regarding the mechanism of potassium dysregulation, Trachtenbarg explains that multiple mechanisms are at work. With osmotic diuresis due to hyperglycemia, much of the serum potassium is lost. Further, acidosis increases serum potassium levels and insulin administration lowers them. Thus, significant shifts occur in the disorder. Once adequate urine output is confirms and the potassium level is less than 5mEq/L, potassium administration should be started due to the usual depletion of total body stores.
Olivieri and Chasm and Wolfsdorf et al. discuss DKA in the pediatric patient. Treatment involves fluid resuscitation, insulin, and electrolyte replacement under constant monitoring for cerebral edema. When DKA is recognized and treated immediately, the prognosis is excellent. Precision in fluid management is vital in pediatric patients who have a higher basal metabolic rate than adults and a larger surface area to volume ratio. Also, since cerebral autoregulation is not as developed in pediatric patients, the risk for cerebral edema is higher.
Illustration A depicts the symptoms of acidosis.
Answer 1: Patients with DKA more often present with hyponatremia. Remember that serum sodium decreases 1.6 mEq/L for every 100 mg/dL increase in glucose.
Answer 3: DKA requires hyperglycemia by definition. Hypoglycemia can be a complication of treatment if glucose is not monitored closely.
Answer 4: Ketones, such as Beta-OH-Butyrate, are commonly found in patients with DKA since ketogenesis is a normal response to starvation caused by inadequate transit of serum glucose into cells.
Answer 5: Patients with DKA present with an anion-gap metabolic acidosis secondary to ketoacids.
Trachtenbarg DE. Diabetic ketoacidosis.Am Fam Physician. 2005 May 1;71(9):1705-14.
PMID:15887449 (Link to Abstract)
Olivieri L, Chasm R. Diabetic ketoacidosis in the pediatric emergency department. Emerg Med Clin North Am. 2013 Aug;31(3):755-73. doi: 10.1016/j.emc.2013.05.004. Epub 2013 Jul 6.
PMID:23915602 (Link to Abstract)
Wolfsdorf J, Glaser N, Sperling MA; American Diabetes Association. Diabetic ketoacidosis in infants, children, and adolescents: A consensus statement from the American Diabetes Association. Diabetes Care. 2006 May;29(5):1150-9.
PMID:16644656 (Link to Abstract)